Congestive heart failure (CHF) has reached an epidemic proportion in the U.S. and worldwide with serious consequences in terms of human suffering and economic impact. In the U.S. alone, there are 60,000 patients dying each year with CHF as the underlying cause. Approximately 5,800,000 Americans have been diagnosed with this condition and this number is increasing every year. In the absence of myocardial infarction, hypertension is a primary risk factor of CHF (D. Lloyd-Jones et al. (2002) Circulation 106: 3068-3072) mainly due to the chronic elevation of the left ventricular (LV) workload and the development of left ventricular hypertrophy (LVH) (W. Kannel et al. (1994) British Heart Journal 72: S3-S9; G. Mitchell et al. (2010) Circulation 121: 505-511; and M. Moser et al. (1996) J Am Coll Cardiol 27: 1214-1218).
Healthy heart function is based on a delicate balance between its pumping capacity (cardiac output, stroke volume) and the input resistance of the receiving vascular system. The pumping mechanism of the heart is pulsatile—with each heartbeat, the heart sends a wave of pressure surge accompanied by local vessel dilation throughout the vascular conduits. The intensity and pulsatility of this pressure and the dilation wave decreases as the waves enter smaller vessels and eventually disappear in the capillary bed. Therefore, wave dynamics dominates the hemodynamics of large vessels such as the ascending, descending and abdominal aorta.
In this respect, vascular resistance in large arteries is composed of a primary viscous component and a dynamic component that is a function of wave characteristics such as frequency (heart beat), amplitude (stroke volume), wave length, and pressure-flow phase difference which depends on the elastic and viscoelastic properties of the carrier vessel. In the electrical circuit terminology, the frequency-dependent component of vascular resistance is known as “impedance.” Essentially, this dynamic resistance is the response of the vascular system as a compliant system to the pressure and wall expansion waves that originate at the root of the aorta during the systolic phase.
It is known (W. Nichols et al. (2005) “McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles”) that pressure wave reflection from branching points (renal arteries etc.), or from sudden changes in the wall properties such as thickness, diameter or stiffness can grossly change the resistance that the heart experiences during the cardiac cycle. Stiffening of the aorta due to aging or vascular diseases, for instance, hampers the ability for blood vessels to vasodilate. This effect is a major source of elevated systemic resistance and thus blood pressure. Such stiffening also results in a change in the wave speed and length of forward propagating waves as well as the nature of their interaction with the reflective waves.
While efforts have been made trying to elucidate the role of wave reflections in heart failure (S. Curtis et al. (2007) Am J Physiol Heart Circ Physiol 293: H557-562; and G F Mitchell et al. (2001) Hypertension 38: 1433-1439), and clinical studies have confirmed that abnormal pulsatile loads play an important role in the pathogenesis of LVH and CHF (Supra G. Mitchell et al. (2010); H. Ooi et al. (2008) Congestive Heart Failure 14: 31-36), conventional cardiology in general ignores this wave dynamic and its impact on the vascular resistance mainly due to the complexity of the wave interaction process. Therefore, there is a need for novel methods and devices that take advantage of recently gained insights in hemodynamics in the treatment and prevention of heart diseases and heart failure.